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. 2018 Oct 23;8:15661. doi: 10.1038/s41598-018-33994-8

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Cellular composition in zebrafish ventricles change following cryoinjury but normalize during regeneration. (A) Absence or weak expression of the cmlc2:GFP transgene in the infarcted myocardium. The infarct (gray region, outlined by the dashed lines in pink) progressively diminished in size during the regeneration process and was nearly or completely undetectable by 35 days post infarct (DPI). BA: bulbus arteriosus. (B–G) Representative histology and TEM images (left) and corresponding quantification (right) of zebrafish ventricles in the days following cryoinjury. For statistical comparison, the biological response to cryoinjury was grouped into three different phases: immediate (0 DPI), remodeling (3 & 7 DPI), and regeneration (14 & 35 DPI). Significant deviations from the extrapolated age-specific baseline mean (dashed horizontal line) was determined Wilcoxon signed-rank test at p < 0.05. (B) Masson trichrome staining (n ≥ 6 per phase, 30 total). During the remodeling phase, there was a decrease in myocardium in both the infarct and non-infarct zones. This was subsequently restored during the regeneration phase. (C) TUNEL staining (n ≥ 3 per phase, 18 total). During the remodeling phase, overall cell and apoptotic cell densities in the ventricle significantly increased. Cell apoptosis was especially apparent in the infarct zone. In the regeneration phase, overall cell density normalized while apoptotic cell density fell to below the baseline mean. (D) CD31 immunostaining (n ≥ 4 per phase, 20 total). The endothelial cell fraction decreased from the immediate to the remodeling phases despite temporarily increasing on 7 DPI; endothelial cell fraction continued to decrease in the regeneration phase. (E) SMA immunostaining (n ≥ 3 per phase, 17 total). The myofibroblast fraction rose from the immediate to the remodeling phase, reaching a maximum at 7 DPI before falling in the regeneration phase. (F) MF20 immunostaining (n ≥ 4 per phase, 22 total). The cardiomyocyte fraction fell precipitously in the remodeling phase, but normalized during the regeneration phase. (G) TEM (n ≥ 15 per time point, 53 total). Significant sarcomere disarray in the infarct and border zone was observed at 0 DPI. No sarcomeres were observed in the infarct zone at 3 DPI but sarcomeres were observed in and around the infarct zone on and after 7 DPI.